Byssinosis is an occupational lung disease associated with the inhalation of cotton and other textile dusts. Based on epidemiologic and clinical investigations, it is likely that the pathogenesis of this illness involves repeated airway inflammation resulting from exposure to agents in mill dust. Using a well established model of the disease, studying healthy volunteers challenged with an extract of cotton bracts, the investigator has shown that exposure to this extract mimics specific features of early byssinosis (e.g., "Monday dyspnea") and confirms the epidemiologic finding that cigarette smoking is a risk factor for more pronounced airway responses. Furthermore, it is demonstrated that a measurable consequence of these episodes of airway inflammation is increased airway reactivity following challenge with cotton bract extracts (CBE). A plausible hypothesis explaining individual susceptibility to the respiratory effects of textile dust exposure, and presumably risk for disease, is that underlying nonspecific airway reactivity determines the degree to which an individual responds to the progressive inflammatory process in byssinosis. A consequence of the hyperactivity hypothesis in byssinosis is that risk factors which enhance reactivity may contribute to the progression of the disease, and moreover, their possible role can be explored in byssinosis using the CBE model. Cigarette smoke, atopic status and baseline reactivity in otherwise healthy non-smokers may affect sensitivity to environmental agents by enhancing airway reactivity. The investigator will study these risk factors by perusing four specific aims, 1) the effect of passive smoking on airway responsiveness following CBE inhalation in healthy non-smokers (HNS), 2) the effect of atopic status on airway responsiveness following CBE in HNS, 3) the effect of baseline non-specific airway reactivity on airway responsiveness following CBE in HNS, and 4) investigations extended in healthy smokers to better define the effects of acute versus chronic exposure to cigarette smoke on airway responsiveness following CBE.